Department of Zoology, University of Gothenburg, Gothenburg, Sweden.
Am J Physiol Regul Integr Comp Physiol. 2010 May;298(5):R1240-8. doi: 10.1152/ajpregu.00781.2009. Epub 2010 Feb 17.
We have studied the potential role of CCK as a regulator/modulator of the postprandial increase in gastrointestinal blood flow. Rainbow trout (Oncorhynchus mykiss) were instrumented with pulsed Doppler flow probes to measure the effects of CCK on cardiac output and gastrointestinal blood flow. Furthermore, vascular preparations were used to study the direct effects of CCK on the vessels. In addition, we used in situ perfused hearts to further study the effects of CCK on the cardiovascular system. When the sulfated form of CCK-8 was injected at a physiological concentration (0.19 pmol/kg) in vivo, there was a significant increase in the gastrointestinal blood flow (18 +/- 4%). This increase in gastrointestinal blood flow was followed by a subsequent increase in cardiac output (30 +/- 6%). When the dose was increased to 0.76 pmol/kg, there was only a 14 +/- 6% increase in gastrointestinal blood flow; possibly due to a dose-dependent increase in the gill vascular resistance as previously reported or a direct effect on the heart. Nevertheless, CCK did not affect the isolated vessel preparations, and thus, it seems unlikely that CCK has a direct effect on the blood vessels of the second or third order. CCK did, however, have profound effects on the dynamics of the heart, and without a change in cardiac output, there was a significant increase in the amplitude (59 +/- 4%) and rate (dQ/dt: 55 +/- 4%; -dQ/dt: 208 +/- 49%) of the phasic flow profile. If and how this might be coupled to a postprandial gastrointestinal hyperemia remains to be determined. We conclude that CCK has the potential as a regulator of the postprandial gastrointestinal blood flow in fish and most likely has its effect by inducing a gastrointestinal hyperemia. The mechanism by which CCK acts is at present unknown.
我们研究了 CCK 作为调节/调制餐后胃肠道血流增加的潜在作用。用脉冲多普勒血流探头给虹鳟（Oncorhynchus mykiss）安置仪器，以测量 CCK 对心输出量和胃肠道血流的影响。此外，还使用血管制剂来研究 CCK 对血管的直接作用。另外，我们使用原位灌流心脏进一步研究 CCK 对心血管系统的作用。当生理浓度（0.19 pmol/kg）的 CCK-8 硫酸盐在体内注射时，胃肠道血流显著增加（18 ± 4%）。这种胃肠道血流的增加随后导致心输出量增加（30 ± 6%）。当剂量增加到 0.76 pmol/kg 时，胃肠道血流仅增加 14 ± 6%；可能是由于先前报道的剂量依赖性鳃血管阻力增加，或者是对心脏的直接作用。然而，CCK 对分离的血管制剂没有影响，因此，CCK 似乎不太可能对第二级或第三级血管有直接作用。然而，CCK 对心脏的动力学有深远的影响，在心输出量没有变化的情况下，相位流量曲线的振幅（59 ± 4%）和速率（dQ/dt：55 ± 4%；-dQ/dt：208 ± 49%）显著增加。这是否以及如何与餐后胃肠道充血相关仍有待确定。我们的结论是，CCK 有可能成为鱼类餐后胃肠道血流的调节剂，并且很可能通过诱导胃肠道充血来发挥作用。CCK 作用的机制目前尚不清楚。
